Implantation of mouse blastocysts does not occur at the expected time if the correct mixture of estrogen and progesterone is lacking; such 'delayed implantation' occurs naturally in lactating females and can be produced experimentally by maternal ovariectomy. The embryos are relatively quiescent metabolically as shown by their low levels of CO2 production and protein synthesis and are 'activated' and induced to implant only by injecting the mother with a combination of estrogen and progesterone. On the other hand, 'dormant' embryos become metabolically 'active' in vitro even in the absence of hormones. Two possible explanations are: 1) a stimulatory milieu is provided by the uterus in response to estrogen and progesterone (and simulated by conditions in vitro); and 2) an inhibitory product is elaborated by the uterus in the absence of estrogen and progesterone and is removed or destroyed by the hormones (the absence of such an inhibitor in vitro would allow the 'dormant' embryos to become 'active'). The overall objective of this work is to define the mechanism by which estrogen and progesterone control embryonic metabolism and thus the initiation of implantation in 'delayed implantation'. The rate of protein synthesis and CO2 production by normal and 'delayed implanting' mouse blastocysts will be measured under various conditions to determine how embryonic metabolism is 'turned on and off'.